ATEROSKLEROSIS

Lina Adilla
15-050
definisi
Kondisi dimana terjadi pengerasan dan
penyempitan pembuluh darah akibat
penebalan tunika intima
Ditandai dengan penimbunan sejumlah
substansi yang terbentuk di dalam lapisan
tunika intima hingga tunika media, yang
disebut sebagai plak ateroma
Komponen plak ateroma
Sel makrofag, leukosit, otot polos
Matriks Ekstra Sel kolagen, serat elastik,
proteglikan
Lemak
Dapat terjadi pada arteri di
Jantung infark miokard
Otak stroke
Ginjal gagal ginjal
Lengan & tungkai gangren
Organ lain disfungsi organ
epidemiologi
Major cause of death and premature disability
in developed societies (IPD harrison, 18th ed)
Banyak ditemukan di sebagian besar negara
maju (patologi robin kumar, ed 7)
Faktor Risiko
Risiko Mayor Risiko Minor, tidak pasti,
Tidak terukur
Tidak dapat dikendalikani: Kegemukan
Usia Kurang gerak
Laki-laki Stres
Riwayat keluarga Defisiensi estrogen pasca
Kelainan genetik menopause
Asupan KH tinggi
Lipoprotein(a)
Dapat dikendalikan : Asupan lemak tak jenuh

Hiperlipidemia Chlamydia pneumoniae
Hipertensi
Merokok
DM
Risk factors of Ath. can be influenced

Hyperlipidemia
Hypertension
Smoking
Diabetes mellitus
Hyperhomocysteinemia.
 Risk factors that cannot be influenced

Age
Male sex
A genetic predisposition
Hyperlipidemia
Kolestrol >265 mg/dL pd usia 3540 th increase
the risk of coronary heart disease.
70% of this cholesterol is transported in low-
density lipoproteins (LDLs) and the development
of Ath. correlates closely with increased LDL
levels.
A defect in LDL receptors leads to very early Ath.
A special risk factor seems to be lipoprotein
Smoking
It is not clear how smoking promotes Ath.
Possible causes are sympathetic nervous
system stimulation by nicotine, displacement
of O2 in the Hb molecule by carbon monoxide,
increased platelet adhesiveness, and raised
endothelial permeability, induced by
constituents in smoke.
Hyper-homocysteinemia.
Due to a lack of methylene tetra hydrofolate
reductase [MTFR], increases the risk of Ath.,.
Homocystein (HoCys) favors plaque formation,
probably in several ways.
Patogenesis
The pathogenesis of Ath. remains
unexplained, but endothelial damage could
be the primary event and the reaction to it
may eventually lead to plaque formation
(response to injury hypothesis).
Plaques usually develop at sites of high
mechanical stress, in this way also
hypertension becomes a risk factor.
 Among the reactions are an increased lipid
uptake in the vessel wall as well as adhesion of
monocytes and thrombocytes helped by
HoCys.
The monocytes penetrate into the intima and
are transformed into macrophages
 These liberate reactive O2 radicals, especially
the superoxide anion O2 (also helped by
HoCys), which have a general damaging effect
on endothelial cells and inactivate
endothelium-formed NO. (inhibition of
platelet and monocyte adhesion to the
endothelium.)
 O2 radicals modify by oxidation of those LDLs
that have entered the endothelium
Oxidized LDLs damage the endothelium and
there induce the expression of adhesion
molecules which allow vessel musculature to
proliferate.
 Oxidation also results in altered binding of LDLs.
They can no longer be recognized by ApoB 100
receptors but rather by so-called scavenger
receptors that are contained in large amounts
within the macrophages.
Consequently, these now phagocytize large
amounts of LDLs and are transformed into
sedentary foam cells (sel busa)
 Simultaneously, chemotactic factors of monocytes and
thrombocytes trigger the migration of smooth muscle
cells from the media into the intima.
Here they are stimulated to proliferate by PDGF and
other growth-promoting factors (from macrophages,
thrombocytes, damaged endothelium, and the muscle
cells themselves).
They, too, are transformed into foam cells by uptake of
oxidized LDLs
They form an extracellular matrix (collagen, elastin,
proteoglycans) that also contributes to atheroma
formation. The consequences of plaque deposition
The consequences of plaque deposition are

Narrowing of the lumen that can lead to ischemia.

Stiffening of the vessel wall (calcification)
Thrombus formation that obstructs the residual
lumen and can cause peripheral emboli
The wall may be stretched and even rupture, with
dangerous bleeding into the surrounding tissues,
for example, from the aorta or cerebral vessels
pencegahan
Primer
Bertujuan untuk menunda pembentukan arteroma
Atau menyebabkan regresi lesi yang sudah
terbentuk pada orang yang belum pernah
menderita penyulit serius PJK arteriosklerotik
Sekunder
Ditujukan untuk mencegah kekambuhan serangan
seperti infark miokardim pd pasien dg penyakit
simptomatik
primer
Dg modifikasi faktor risiko
Tidak merokok
Mengendalikan hipertensi
Managemen stres
Menurunkan BB
Memperbanyak Olahraga
Konsumsi makanan rendah lemak jenuh
 sumber
Harrisons Principles of Internal Madecine
18th ed
Patologi robin kumar vol 2 edisi 7
Patofisiologi silbernagl